1. Field of the Invention
The present invention relates to a heart treatment equipment and method for preventing a sudden cardiac death caused by a fatal arrhythmia in patients with an organic heart disease.
2. Description of the Related Art
FIGS. 17A and 17B show a constitutional diagram of a heart and an electrocardiogram waveform respectively. A heart is constituted by two atriums and two ventricles. The atriums are chambers for storing the returned blood and the ventricles are chambers for ejecting the blood. With respect to the blood, the venous blood enters the right atrium through a large vein and is sent to a pulmonary artery passing through the right atrium and the right ventricle. The arterial blood which takes in oxygen in lungs goes into a left atrium through the pulmonary vein and is sent to the aorta passing through the left atrium and the left ventricle. The thickness of the ventricle is thicker than that of the atrium, and additionally, in order to prevent backflow of the blood, valves are provided between the right atrium and the right ventricle, between the right ventricle and the pulmonary artery, between the left atrium and the left ventricle and between the left ventricle and the aorta respectively. The condition where the heart loses its ability to maintain adequate blood circulation in the peripheral tissues and the lungs is a heart failure and in many cases, left heart failure where the pumping ability of the left ventricle is primarily affected.
Though there are individual differences, the beating of the heart counts about 100,000 times in a day. Then, a weak current is emitted every beat of the heart, so that it is possible to know the condition of the heart by detecting this current. An electrocardiogram of FIG. 17B shows a time course of the electrical activity of the normal heart. This electrocardiogram is obtained from electrodes placed on the skin in specific locations and is consisting of a plurality of waves which have amplitudes of several millivolts. As shown in the drawing, first, a wave which comes first is a P wave and this represents a current in a case when the atria (the right atrium and left atrium) depolarize. The wave which comes next is a wave called as a QRS complex and this is a wave of ventricular depolarization.
A PQ interval begins at the onset of the P wave and to the onset of the QRS complex and represents the time between the start of atrial depolarization and the start of the ventricular depolarization. A QT interval begins at the onset of the QRS complex and to the end of the T wave and represents the time between the start of ventricular depolarization and the end of ventricular repolarization.
A sudden death especially caused by a heart disease is called a sudden cardiac death and the number thereof reaches about annual 50,000 people in Japan. The immediate cause of the sudden cardiac death is the life-threatening ventricle tachycardia or the ventricle fibrillation and which is called a fatal arrhythmia. When the ventricle tachycardia which is defined as a heart rate over 100 beats/min or the ventricle fibrillation which is extremely rapid chaostic heartbeat occurs, the pumping function of the heart lowers or disappears and it becomes impossible to fill with enough blood to supply the whole body with the oxygen rich blood that it needs. For this reason, unconsciousness is caused in accordance with the decrease in the cerebral blood flow, so that a death might be caused unless an immediately appropriate treatment is conducted. The organic heart disease patients who are suffered with myocardial infarction, cardiomyopathy and the like are at high risk of the ventricle tachycardia and the ventricle fibrillation.
For a patient having a risk of such a sudden cardiac death, an implantable cardioverter defibrillator (ICD) is used. When a ventricle tachycardia or a ventricle fibrillation is detected, the ICD delivers a shock to the heart in order to interrupt the rapid heart rhythm and restore a more normal rhythm. However, a high-energy shock is required for defibrillation and there is a danger that the cardiac tissue subjected to the shock could be damaged.
Moreover, an anti-arrhythmic medicine is generally used in order to prevent a sudden cardiac death. Especially, for the organic heart disease patients with reduced left ventricle function, it is being confirmed by cardiovascular trials in the United States that a β-blocker medicine or a class III anti-arrhythmic medicine with a β-blockade effect has an effect on the reduction of mortality. The β-blocker medicine has an effect on mainly lowering a heart rate and is effective for suppressing a rapid heart rate.
In this way, by lowering the heart rate, it is possible to reduce the number of the risk event which includes a ventricle tachycardia or a ventricle fibrillation such as a ventricular premature contraction and the like and additionally, by the decrease of the oxygen consumption of the cardiac muscle owing to the lowering of the heart rate, it is considered that it is possible to prevent a myocardial infaction and at the same time prevent a myocardial failure region and its peripheral region from becoming oxygen-deprived.
Now, the cardiac activity is put under the control of an autonomic nerve system and the autonomic nerve system has a sympathetic nerve system and a parasympathetic nerve system where the parasympathetic nerve system of the heart is a vagus nerve. The activities in the sympathetic nerve and the vagus nerve are usually antagonistic each other. The cardiac activity. (mainly heart rate and contractility) increases when the sympathetic tone increases and the cardiac activity (mainly heart rate) decreases when the vagal tone increases.
More specifically, the increase in the sympathetic tone has an excitatory effect on the cardiac activity and on the other hand, the increase in the vagal tone has an inhibitory effect on the cardiac activity. When the sympathetic tone is activated and the sympathetic tone is made to be high, a possibility of a fatal arrhythmia increases. The sympathetic tone is generally activated by physical stress or mental stress. The β-blocker medicine acts on the sympathetic nerve and makes the tone thereof calm down, so that it is considered that it is effective to prevent the fatal arrhythmia.
Additionally, it is known that the electrical stimulation of the vagus nerve exerts a similar action as the blocker medicine. Based on this principle, a method was proposed where the tachyarrhythmia is prevented or stopped by electrically stimulating the vagus nerve when a tachyarrhythmia is detected (see, for example, the specification of JP OP 8-38625).
Further, an equipment for detecting an arrhythmia in response to an activity of a nerve signal which transmits information from the autonomic nerve system to the heart has been also proposed (see, for example, the specification of JP OP 8-52121). This arrhythmia detecting equipment comprises a sensor for detecting a nerve activity and a comparator provided with a threshold value for forming a condition with reference to an existence of the arrhythmia wherein the comparator outputs an output which shows a generation of the arrhythmia depending on whether or not the nerve activity is in conformity to the condition. More specifically, the vagus nerve is lightly activated for 5 seconds immediately after an impeding fibrillation or some other dangerous impeding tachyarrhythmia is detected based on a change in the activity of an autonomic nerve system and the like. Then, the treatment will be terminated when detecting a return to a normal state of the heart and the treatment will continue, supplemented with blocking of the sympathetic nerve, preferably at the ganglion stellatum for a few seconds when detecting an abnormal condition for the heart continuously. In a case when the heart activity drops below a given rate owing to a fact that a current is supplied to the vagus nerve and the sympathetic nerve, the pacemaker block starts the stimulation of the heart automatically in order to maintain or restore its sinus rhythm.
Furthermore, in order to avoid the fatal arrhythmia, it is proposed a method and an equipment where an electrical stimulation is applied to the vagus nerve (see, for example, WO93/21824 <PCT/US93/00051>). In this equipment for treating the arrhythmia, it is directed to prevent a tachycardia or a fibrillation beforehand by detecting an ST segment change (voltage) of the patient's electrogram and by emitting a trigger for a nerve stimulation whether or not the ST value exceeds the threshold value. Further, an appropriate function of the heart would be maintained by means of the stimulation of the heart and the stimulation of the vagus nerve. This heart treatment equipment not only compares a pre-set interval threshold for detecting the tachycardia with the cardiac interval of the patient, but also carefully examines the ST segment change (voltage) of the electrogram indicative of an acute myocardial ischemia and other contributing factors relating to the ventricle tachycardia such that it becomes possible to prevent the tachycardia based on that result. Additionally, at the same time in order to overcome the decrease in the heart rate owing to the vagus nerve stimulation, the stimulation is applied to the heart for making the patient's heart rate be in a tolerance range. The arrhythmia treatment equipment is constituted by means for continuously measuring an electrogram, means for detecting a characteristic of the aforesaid electrogram indicative of the tachycardia, means for initializing memories of a series of characteristics, means for supplying one or more electrical stimulations to a patient nerve system, and means for initializing a series of characteristics of the electrogram subsequent to the stimulation of the vagus nerve.
If an excessive stimulation of the vagus nerve is performed, there is a problem that side-effects such as an influence to the organs other than the heart become remarkable where, for example, dyspepsia and nausea owing to an excessive secretion of gastric acid, insulin, glucagons and the like or cough increase, pharyngitis, laryngismus, paresthesia, dyspnea and induction of an asthmatic attack for patients with a history of asthma patient will be induced, and if an enough stimulation of the vagus nerve is not performed conversely, there is a problem that enough effect cannot be obtained.